中山大学学报（医学科学版）
中山大學學報（醫學科學版）
중산대학학보（의학과학판）
JOURNAL OF SUN YAT-SEN UNIVERSITY(MEDICAL SCIENCES)
2004年
6期
493-495,503
,共4页
区景松%Kirkwood A.Pritchard Jr
區景鬆%Kirkwood A.Pritchard Jr
구경송%Kirkwood A.Pritchard Jr
热休克蛋白 90%一氧化氮合酶%一氧化氮%氧自由基%内皮
熱休剋蛋白 90%一氧化氮閤酶%一氧化氮%氧自由基%內皮
열휴극단백 90%일양화담합매%일양화담%양자유기%내피
heat shock protein 90%nitric oxide synthase%nitric oxide%superoxide%endothelial cell
阐述热休克蛋白 90( hsp90)作为一个心血管疾病新的调节物,在调节内皮一氧化氮合酶( eNOS)功能方面的作用:血管内皮一氧化氮( NO)主要来源于 eNOS; eNOS同时有产生 NO和氧阴离子自由基(O2)的功能. NO与(O2)的平衡在调节心血管方面有着重要的作用,当这个平衡被打破时可导致多种心血管疾病的发生发展;实验发现,当 hsp90与 eNOS结合增加时, eNOS耦联产生 NO,当 hsp90与 eNOS结合减少或结合后无发生结构改变时 eNOS非耦联产生(O2) .进而提出深入探讨 hsp90调节 eNOS机制的必要性.
闡述熱休剋蛋白 90( hsp90)作為一箇心血管疾病新的調節物,在調節內皮一氧化氮閤酶( eNOS)功能方麵的作用:血管內皮一氧化氮( NO)主要來源于 eNOS; eNOS同時有產生 NO和氧陰離子自由基(O2)的功能. NO與(O2)的平衡在調節心血管方麵有著重要的作用,噹這箇平衡被打破時可導緻多種心血管疾病的髮生髮展;實驗髮現,噹 hsp90與 eNOS結閤增加時, eNOS耦聯產生 NO,噹 hsp90與 eNOS結閤減少或結閤後無髮生結構改變時 eNOS非耦聯產生(O2) .進而提齣深入探討 hsp90調節 eNOS機製的必要性.
천술열휴극단백 90( hsp90)작위일개심혈관질병신적조절물,재조절내피일양화담합매( eNOS)공능방면적작용:혈관내피일양화담( NO)주요래원우 eNOS; eNOS동시유산생 NO화양음리자자유기(O2)적공능. NO여(O2)적평형재조절심혈관방면유착중요적작용,당저개평형피타파시가도치다충심혈관질병적발생발전;실험발현,당 hsp90여 eNOS결합증가시, eNOS우련산생 NO,당 hsp90여 eNOS결합감소혹결합후무발생결구개변시 eNOS비우련산생(O2) .진이제출심입탐토 hsp90조절 eNOS궤제적필요성.
The aim of this article was to illustrate the effect of regulation of endothelial nitric oxide synthase (eNOS) by heat shock protein 90 (hsp90), a newly recognized player in cardiovascular diseases. eNOS is the major source of nitric oxide (NO) in vascular endothelial cells. eNOS has two activities, producing NO and generating superoxide anion (O2). The balance between NO (O2) and may play important roles in regulating cardiovascular system. Disturbances in this balance may lead to many cardiovascular diseases. When increase of hsp90 associated with eNOS, eNOS couples and generates NO, when decrease of hsp90 associated with eNOS or no changes on hsp90 conformation after associated with eNOS, eNOS uncouples and generates (O2). It is necessary to understand how hsp90 regulates eNOS in the future.
